Evidence map›Paper›PMID 24912092›Full record

ArticleJournal of cellular physiology2015

Histone deacetylase inhibition destabilizes the multi-potent state of uncommitted adipose-derived mesenchymal stromal cells.

Amel Dudakovic, Emily T Camilleri, Eric A Lewallen, Meghan E McGee-Lawrence, Scott M Riester, Sanjeev Kakar, Martin Montecino, Gary S Stein, Hyun-Mo Ryoo, Allan B Dietz and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Potential to Fight Obesity with Adipogenesis Modulating Compounds.International journal of molecular sciences · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Amel DudakovicDepartment of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota.
Emily T Camilleri
Eric A Lewallen
Meghan E McGee-Lawrence
Scott M Riester
Sanjeev Kakar
Martin Montecino
Gary S Stein
Hyun-Mo Ryoo
Allan B Dietz
Jennifer J Westendorf
Andre J van Wijnen
Mayo Clinic · USSeoul National University · KRUniversidad Andrés Bello · CLUniversity of Vermont · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
SUBNUCLEAR TARGETING OF TRANSCRIPTION FACTORSP01CA082834 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STEIN, GARY S. · 2001 to 2015
$18.4M
CONTROL OF OSTEOBLAST PROLIFERATION AND DIFFERENTIATIONR01AR039588 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B., STEIN, GARY S. · 1990 to 2019
$8.0M
Molecular Control of Bone FormationR01AR049069 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WESTENDORF, JENNIFER J · 2003 to 2021
$5.8M
Runx2 and Axin2 Interactions During Bone FormationR01DE020194 · NIDCR · MAYO CLINIC ROCHESTER · PI WESTENDORF, JENNIFER J · 2010 to 2014
$2.1M
NCATS NIH HHS UL1 TR000135NCI NIH HHS CA082834NCI NIH HHS P01 CA082834NIAMS NIH HHS R01 AR039588NIAMS NIH HHS R01 AR049069NIDCR NIH HHS R01 DE020194
6 · The paper itself

Abstract

Human adipose-derived mesenchymal stromal cells (AMSCs) grown in platelet lysate are promising agents for therapeutic tissue regeneration. Here, we investigated whether manipulation of epigenetic events by the clinically relevant histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) alters differentiation of AMSCs. The multipotency of AMSCs was validated by their ability to differentiate into osteogenic, chondrogenic, and adipogenic lineages. High-throughput RNA sequencing and RT-qPCR established that human histone deacetylases (HDAC1 to HDAC11, and SIRT1 to SIRT7) are differentially expressed in AMSCs. SAHA induces hyper-acetylation of histone H3 and H4, stimulates protein expression of the HDAC-responsive gene SLC9A3R1/NHERF1 and modulates the AKT/FOXO1 pathway. Biologically, SAHA interferes with osteogenic, chondrogenic and adipogenic lineage commitment of multipotent AMSCs. Mechanistically, SAHA-induced loss of differentiation potential of uncommitted AMSCs correlates with multiple changes in the expression of principal transcription factors that control mesenchymal or pluripotent states. We propose that SAHA destabilizes the multi-potent epigenetic state of uncommitted human AMSCs by hyper-acetylation and perturbation of key transcription factor pathways. Furthermore, AMSCs grown in platelet lysate may provide a useful biological model for screening of new HDAC inhibitors that control the biological fate of human mesenchymal stromal cells.

Indexed as

AcetylationAdipocytesAdipose TissueBase SequenceCell DifferentiationCells, CulturedChondrocytesForkhead Box Protein O1Forkhead Transcription FactorsGuided Tissue RegenerationHigh-Throughput Nucleotide SequencingHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHydroxamic AcidsForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsPhosphoproteinsProto-Oncogene Proteins c-aktsodium-hydrogen exchanger regulatory factorSodium-Hydrogen ExchangersVorinostat

Identifiers

PMID24912092
PMCPMC4225068
OpenAlexW1509831319

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.